Effects of 28 days of beta-alanine and creatine monohydrate supplementation on aerobic power, ventilatory and lactate thresholds, and time to exhaustion.

The effect of beta-alanine (beta-Ala) alone or in combination with creatine monohydrate (Cr) on aerobic exercise performance is unknown. The purpose of this study was to examine the effects of 4 weeks of beta-Ala and Cr supplementation on indices of endurance performance. Fifty-five men (24.5 +/- 5.3 yrs) participated in a double-blind, placebo-controlled study and randomly assigned to one of 4 groups; placebo (PL, n = 13), creatine (Cr, n = 12), beta-alanine (beta-Ala, n = 14), or beta-alanine plus creatine (CrBA, n = 16). Prior to and following supplementation, participants performed a graded exercise test on a cycle ergometer to determine VO(2peak), time to exhaustion (TTE), and power output, VO(2), and percent VO(2peak) associated with VT and LT. No significant group effects were found. However, within groups, a significant time effect was observed for CrBa on 5 of the 8 parameters measured. These data suggest that CrBA may potentially enhance endurance performance.

Effects of an external nasal dilator on the work of breathing during exercise.

PURPOSE: The effect of an external nasal dilator on the work of breathing (WOB) was measured during exercise in 14 untrained college students (age, 23 +/- 2.7 yr). METHODS: Two maximal, incremental ergometer tests were performed to exhaustion. Subjects wore a placebo or an active nasal dilator strip, in random order, during each test. An esophageal balloon was placed through each of the subject's mouth into the esophagus for measurement of inspiratory elastic work (INEW), inspiratory resistive work (INRW), and expiratory resistive work (EXRW). Subjects breathed through a Hans Rudolph(R) face mask that covered both the mouth and nose during both tests. Measured variables included oxygen uptake (VO2), ventilation (VE), tidal volume (VT), frequency of breathing (f), INEW, INRW, and EXRW (work expressed in joules). An alpha level was set at P < 0.05. RESULTS: No significant differences were found in INEW, INRW, and EXRW between conditions at 70% of VO2max (mean +/- SD; Placebo: INEW, 25.6 +/- 17.8 J.min-1; INRW, 22.4 +/- 15.8 J.min-1; EXRW, 16.7 +/- 12.3 J.min-1; Active: INEW, 24.7 +/- 12.9 J.min-1; INRW, 19.7 +/- 11.9 J.min-1; EXRW, 15.2 +/- 8.6 J.min-1; P > 0.05). No difference was found in INEW, INRW, and EXRW at maximal exercise between conditions (mean +/- SD; Placebo: INEW, 50.2 +/- 29.9 J.min-1; INRW, 67.3 +/- 42.3 J.min-1; EXRW, 102.3 +/- 78.4 J.min-1; Active: INEW, 45.7 +/- 19.6 J.min-1; INRW, 62.6 +/- 36.7 J.min-1; EXRW, 86.3 +/- 50.9 J.min-1; P > 0.05). There were no differences in VO2, VE, VT, or f between conditions. CONCLUSION: Wearing an external nasal dilator does not significantly reduce the work of breathing during exercise.

Oxygen uptake and ventilatory effects of an external nasal dilator during ergometry.

INTRODUCTION: Athletes and coaches have begun to use external nasal dilators with the perception that they enhance performance and make it "easier to breathe." This study was conducted to ascertain whether application of an external nasal dilator would enhance performance, as measured by maximal oxygen uptake (VO2max), maximal ventilation (V(Emax)), maximal work rate (Wr(max)) or ratings of perceived exertion and dyspnea (RPE, RPD). METHODS: Fifteen subjects (F = 10; M = 5: age, 20+/-1.4, mean +/- SD) performed three incremental exercise tests to fatigue on an ergometer at 1-wk intervals in randomized order. One test was conducted without a nasal dilator, using a nose clip and mouthpiece for oxygen uptake and ventilatory measurements (control, C). The other two tests used a Rudolph 8900 breathing mask that included the nose in the breathing circuit and subjects wore either a placebo (P) or the active dilator (A). RPE for total body (20-point scale) and for dyspnea (10-point scale) were also measured on all tests. RESULTS: There were no significant differences in VO2max (mean +/- SD; C = 3.12+/-1.1; P = 3.12 + 1.06; A = 3.04+/-0.94). V(Emax) (C = 117+/-26; P = 125+/-31; A = 122+/-26), Wr(max) (C = 256+/-73; P = 255+/-70; A = 257+/-74), RPE (C = 18.8+/-1.78; P = 18.9+/-1.33; A = 18.9+/-1.22), or RPD (C = 9.1+/-1.58; P = 9.3+/-1.2; A = 9.13+/-1.2) during exercise between any group. CONCLUSION: Thus, it is concluded that an external nose dilator does not enhance performance as measured by VO2max, V(Emax), Wr(max), or perceived performance as measured by RPE and RPD.

Airflow limitation and control of end-expiratory lung volume during exercise.

To test the hypothesis that the presence of airflow limitation (AFL) influences the control of end-expiratory lung volume (EELV) during exercise, 11 subjects with normal lung function, performed submaximal exercise (SM) on a cycle ergometer, with and without AFL. AFL was achieved during exercise by increasing the density of the air via a hyperbaric chamber, compressed to a depth of 3 atm (3 ATA; with AFL). Five subjects achieved AFL during SM exercise at 3 ATA while the remaining six subjects did not achieve AFL. SM exercise was performed with the same apparatus in the hyperbaric chamber at sea level pressure with none of the subjects achieving AFL (SL; no-AFL). EELV (% of TLC, BTPS), was significantly larger during exercise at 3 ATA than during exercise at SL for the AFL group (SL = 44 +/- 6%; 3 ATA-AFL = 51 +/- 9%, P < 0.05; but, was not for the no-AFL group (SL = 46 +/- 6%; 3 ATA-no AFL = 46 +/- 7%). End inspiratory lung volume was significantly elevated during exercise at 3 ATA compared with SL in the AFL group (SL = 80 +/- 6%; 3 ATA-AFL = 86 +/- 6%; P = 0.01) but not in the no-AFL group (SL = 82 +/- 4%; 3 ATA-no AFL = 84 +/- 4%). Tidal volume and ventilation were not different for any condition. These data suggest that the occurrence of AFL influences the control of EELV.

Effects of lower body pressure changes on pulmonary function.

PURPOSE: During and following exercise there are a number of changes in pulmonary function, among which is a decrease in forced vital capacity (FVC). Several potential mechanisms may explain this decreased FVC, including an exercise-induced increase in thoracic blood volume. METHODS: We tested the hypothesis that altered thoracic blood volume alone, as produced by the application of 30 mm Hg lower body negative (LBNP) or positive pressure (LBPP) for 5 min, would change FVC and forced expiratory volume in 1 s (FEV1.0). Further, we tested whether the changes in pulmonary function were related to initial lung volume and whether the lower body pressure changes led to an altered lung compliance as measured by static pressure-volume curves. RESULTS: Results indicated that with LBNP, FVC, and FEV1.0 were significantly increased by approximately 0.15 L and 0.18 L, respectively. When LBPP was applied, FVC and FEV1.0 were decreased by approximately 0.18 and 0.14 L, respectively. The increase in FVC with LBNP was significantly related to the original FVC (r = 0.66, P < 0.05). There was no significant correlation between the increase in FEV1.0 and the original FEV1.0 (r = 0.48, P > 0.05). Pulmonary compliance was not changed significantly by the application of LBPP. CONCLUSIONS: These results suggest that part of the change in pulmonary function following heavy exercise is related to an increased thoracic blood volume. The lack of change in lung compliance suggests that the effect of altered thoracic blood volume is to displace air and not to change the mechanical properties of the lungs.

Effects of inspired O2 and CO2 on ventilatory responses to LBNP-release and acute head-down tilt.

Increases in blood flow and CO2 return to the heart and lungs at the onset of exercise have been proposed to initiate reflexive feedback which increases ventilation (VE), via mechanoreceptors in the heart and/or intrapulmonary CO2 flow receptors. Both lower body negative pressure (-40 mm Hg) release (LBNP-release) and acute head-down (-30 degrees) tilt (TILT) provide physiological models to focus upon the effects of increased venous return and CO2 flow on VE, without the confounding influence of limb afferents or the descending efferents associated with central command. We examined the ventilatory responses to LBNP-release and TILT while inhaling one of four gas mixtures: a) room air (R); b) 95% O2 (O); c) 95% O2, 1.25% CO2 (LC); and d) 95% O2, 2.25% CO2 (HC). Breath-by-breath measurements for VE end-tidal CO2 (PETCO2), tidal volume (VT), and breathing frequency (fB) were taken. VE and VT for HC were significantly higher (p < 0.05) than those for R, O, and LC throughout the test session, while fB and PETCO2 were not significantly different among the gas treatments. VE increased (p < 0.05) above resting baseline with LBNP-release and TILT for R, O, LC, and HC primarily through an elevation of fB. Further, the maximal change in VE following LBNP-release or TILT were not different among inhaled gas mixtures. However, area under the VE curve following LBNP-release and TILT was higher for HC compared to the other gas mixtures. We conclude that these results are inconsistent with the theory that carotid bodies are essential in driving VE with these models.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory work and oxygen consumption during exercise and hyperventilation.

The work of breathing (WB), and thus the energy requirement of the respiratory muscles, is increased any time minute ventilation (VE) is elevated, by either exercise or voluntary hyperventilation. Respiratory muscle O2 consumption (VRMO2) in humans has generally been estimated by having subjects breathe at a level comparable to that during exercise while the change in O2 consumption (VO2) is measured. The difference between VO2 at rest and during hyperventilation is attributed to the respiratory muscles and is assumed to be similar to VRMO2 during exercise at the same VE. However, it has been suggested that WB differs between exercise and hyperventilation and that WB during exercise is lower than during hyperventilation at the same VE. In this study we measured WB during exercise and hyperventilation and from these measurements estimated VRMO2. WB, VE, and VO2 were measured in five male subjects during rest and during exercise or hyperventilation at levels of VE ranging from 30 to 130 l/min. VE/WB relationship was determined for both hyperventilation and exercise. Multiple regression analysis showed that the shape of the two curves was different (P < 0.0001), with WB at high levels of VE being < or = 25% higher in hyperventilation than in exercise. In a second study in which frequency, tidal volume, and duty cycle were controlled as well as VE, there was no difference in WB between exercise and hyperventilation. VO2 was significantly correlated with WB, and the estimated VRMO2 did not increase as a fraction of total VO2 as exercise intensity rose.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of flow and resistive training on respiratory muscle endurance and strength.

This study was conducted to ascertain whether resistive or flow type training would better improve both strength and endurance in the respiratory muscles of healthy subjects. Subjects performed a battery of respiratory strength and endurance tests before and after training, which consisted of either control, cycling exercise (E), inspiratory loading (IL), expiratory loading (EL), or hyperventilation (H) training for 4 weeks. Maximal sustained ventilation increased after training in the E and H groups. Both IL and H improved inspiratory fatigue resistance. IL improved maximal inspiratory pressure. No significant changes were found in maximal expiratory pressure although E, EL, and H tended to improve. There was no statistical difference in maximal voluntary ventilation between groups after training, but the H group alone did increase. This study suggests that respiratory muscle strength and endurance can be improved with flow or resistive training. Flow type training improves both flow and resistive tests while resistive training appears to affect only strength and resistive type measurements.

Pulmonary function changes following exercise.

Many studies have documented differing changes in forced vital capacity (FVC) following various intensities and durations of exercise. This investigation used three different intensities and durations of treadmill running, with subjects who were active runners, with the intent of finding an intensity or duration that might elicit changes in FVC and if these changes are related to respiratory muscle fatigue. Intensities and durations included a graded maximal test to exhaustion (7-14 min); a 7-min test at 90% of maximal VO2, and a 30-min test at 60% of maximal VO2 (intensity). Maximal inspiratory pressures (MIP), maximal expiratory pressures (MEP), forced expiratory volume in 1 s (FEV1.0) and FVC were measured pretest, and 5, 10, and 30 min post-test (time). MIP was not different across time or intensities. The decrease in MEP approached significance at 10-min post-exercise compared to pretest values (P = 0.0569), with no differences found between intensities. FVC was different between times (P = 0.0117) but not between intensities. FVC was decreased at 5 and 10 min post-test compared with pre and 30 min. FEV1.0 was significantly reduced at 5 and 10 min post-test compared with pretest. These data suggest that a combination of duration and intensity may be necessary to elicit pulmonary function changes after exercise and that expiratory muscle fatigue may be a factor that results in a reduced FVC.